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IAHI Block 1 > 14 - Kinetoplatid and Protozoa STDs > Flashcards

14 - Kinetoplatid and Protozoa STDs Flashcards

1
Q

What are kinetoplastids? Why are they described this way?

What are the two genera?

A

Obligate intracellular parasites.

Kineplast: disk-shaped, DNA-carrying organelle within the mitochondria. (originally thought to be a motor)

Two genera: Trypanosoma and leishmania

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2
Q

What are the four developmental stages of kinetoplastids? Which one looks different from the others and why?

A

Trypomastigote

Amastigote: flagellum deemphasized relative to other stages because this is the INTRAcellular stage so it doesn’t need the flagellum as much.

Promastigote

Epimastigote

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3
Q

What is the vector of Leishmania? What are the reservoirs?

A

Female sandfly for phlebotomus and lutzomyia.

Resoervoirs: rodents, opossums, anteaters, sloths, cats, dogs. Someimes humans.

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4
Q

Leishmania collectively causes diseases called what? Name them.

A

Leishmaniasis:

  1. Cutaenous (oriental sore)-most common
  2. Mucocutaenous/mucosal-least common
  3. Visceral (kala-azar/black fever)-most serious
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5
Q

How do humans get Leishmaniasis? What is the immune systems role in this?

A

Sandfly takes a blood meal and injects promastigote into the skin.

Promastigotes are phagocytized by macrophages .

Promastigotes turn into amastigotes which multiply in tissues and infect other cells.

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6
Q

What are the significant organisms cause the Cuteaneous leishmaniasis?Where are these found geographically? What is the pathology?

A

L. tropica and L. major

West central africa, middle east, asia minor to india.

Sores in weeks to months, graduate to ulcers, secondary bacterial infections common.

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7
Q

What organisms cause Visceral Leishmaniasis (VL)? What is the geographical distribution? What is the associated pathology?

A

L. donovani and L. infantum (chagasi); 90% in bangladesh,brazil, india, nepal, and sudan.

Can be asymptomatic or rapidly fatal. Illness in months to yrs after infection. Infection of macrophages leads to fever, hepatosplenomegaly, bone marrow deregulation.

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8
Q

What can persistence of visceral leishmaniasis (VL) lead to?

A

Post-kala0azar dermal leishmaniasis or PKDL which is characterized by deeply pigmented granulomatous lesions of the skin that can lead to human to human infection if a sand fly bites them.

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9
Q

Visceral leishmaniasis and HIV are common co-infections in which populations?

A

Most common among IV drug users and people in sourthern europe (particularly spain).

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10
Q

What organism causes mucocutaneous leishmaniasis? What is the geographical distribution? What is the associated pathology?

A

L. braziliensis complex (closely related species)

90% of cases in bolivia, brazil, and peru

Consequence of cutaneous leishmaniasis; spread from the skin to the mucous membranes of the nose, mouth, or throat causing destruction of mucous membranes and secondary infections.

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11
Q

How is Leishmeniasis diagnosed? How is it prevented?

A

Giemsa stain of amastigotes (the ones without flagella) of infected tissues, ie skin sores for cutaneous and mucocutaneous and bone marrow for visceral leichmaniasis.

Prompt treatment, control of reservoir hosts, insect vector control and avoidance.

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12
Q

What are the two types of trypanosoma?

A

African trypanosomiases (african sleeping sickness): T. brucei gambiense and T. brucei rhoesiense

American trypanosomiases (chagas) caused by T. cruzi

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13
Q

What are the geographical locations of T. brucei gambeinse and T. brucei rhodesiense that cause Sleeping sickness? What is the reservoir of each? What spreads them?

A

Gambiense: West/central africa, human reservoir

Rhodesiense: East africa (Cattle raising areas, cattle, sheep, and antelope are the reservoirs.

Tsetse fly spreads both.

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14
Q

Describe the pathology caused by T. brucei gambeinse and T. brucei rhodesiense?

A

Gambiense: chronic; ending fatally with CNS involvement after 1-2 years. Death and coma from secondary infection. Early signs are ulcer at bite site and swollen cervical lymph node (winterbottom sign).

Rhodesiense: Acute; fevers, rigors, myalgia. Progresses to rapidly fatal disease with CNS involvement early. Death within 12 months. More virulent.

Both have 100% mortality when untreated.

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15
Q

Who is at risk for T. brucei gambeinse and T. brucei rhodesiense?

A

Gambiense: living in rural areas near shaded streams.

Rhodesiense: living near cattle-raising areas.

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16
Q

How do humans get T. gambiense?

A

Tsetse fly takes blood meal and injects metacyclic trypomastigotes which transform in the blood and are carried to other sites.

They multiply by binary fission in body fluids.

17
Q

How do we diagnose T. brucei gambiense?

A

Trypomastigotes in blood.

18
Q

Well over 90% of all cases of African Sleeping Sickness are caused by what?

A

The west african Gambiense varity.

19
Q

How does African Trypanosomiasis evade the immune system?

A

Antigenic variation (parasite never eliminated)

Without chemical intervention, you will never get able to get ride othe parasite because it can escape antibodies on the immune system.

20
Q

How would you diagnose T. brucei gambeinse and T. brucei rhodesiense?

A

Microscopy

Rhodesiense readily found in blood (greater parasitemia levels than gambiense)

Gambiense identified from lymph node aspirate from posterior cervical node.

21
Q

What is the first and second stage of african trypanosomiasis?

A

First: acute blood and lymphatic stage

Second: CNS involvement

22
Q

What does Trypanosoma cruzi cause ? What is the vector?

A

American trypanosomiasis (chagas disease).

Vectors are triatomine (Reduviid) bugs caleld kissing bugs.

23
Q

Where do the trypoastigotes and amastigotes of T. cruzi go in the body? How are they transmitted?

A

Trypomastigotes in the blood, intracellular amastigotes in the lymph node and tissues.

Transmitted from bug, congenital, contaminated blood products, organ transplant.

24
Q

What is the epidemiology of american trypanosomiasis? How is it prevented/controlled?

A

Endemic through mexico, central and south america.

300,000 people with it in the US.

Bug control, destroy nets, screening blood products.

25
Q

How do humans contract chagas disease?

A

Triatomine bug takes blood meal and passes metacyclic trypomastigotes in feces which enter the bite wound or mucous membranes.

These penetrate cells and transform into amastigotes that multiply in the tissues and become trypomastigotes that burst out of the cell into the blood.

26
Q

What is the acute pathology of american trypanosomiasis?

A

Acute: less than 8 weeks

  • chagoma: erythematous area near bite
  • Romana sign (rash and edema on upper and lower eyelid
  • circulating trypomastigotes
27
Q

What is the chronic intermediate and chronc pathology of american trypanosomiasis?

A

Chronic intermediate: 8-10 wks post infection: asymptomatic phase with no circulating trypomastigotes.

Chronic: 10-20 years later

  • hepatosplenomegaly, myocarditic, enlarges esophagus and colon
  • CNS involvement, death from tissue damage or heart attack
  • no circulating trypomastigotes but persistant amastigotes.
28
Q

How is the acute and chronic stage of trypanosomiasis (chagas) each diagnosed?

A

Acute: trypomastigotes in thick or thin blood films

Chronic: biopsy of lymph nodes, liver, spleen, or bone marrow for amastigotes.

29
Q

What is trichomoniasis? What are the infected sites? What is the infective stage?

A

STD protozoan caused by trichomonas vaginalis.

Infected sites: UG tract; vagina, urethra, prostate, seminal vescicle, urethra.

Infective stage: trophozoite.

30
Q

How is trichomonas vaginalis transmitted? prevented?

A

Transmitted via sexual intercourse.

Prevention using condoms and not sharing sex toys.

31
Q

What is the pathology and epidemiology of trichomoniasis?

A

Worldwide, #1 curable sexually transmitted disease.

Females causes vaginitis with frothy white or green discharge.

Men freq. asymptomatic but may have urethritis and prostatitis.

32
Q

How do you diagnose trichomoniasis?

A

Giemsa staining of trophozoites in secretions or in vitro culture made by vaginal irrigation.

33
Q

What is imperative in all cases of african trypanosomiasis?

A

CSF testing, because CNS involvement affects treatment options.

34
Q

Why are there concerns about a potential increase in vector-borne cases of T. cruzi in the US?

A

Because the parasite and vector are present; 14 species of mammals are carriers.

35
Q

What are the clinical features of T. vaginalis?

A

Asymptomatic to symptomatic for men and women.

Men: painful urination and ejaculation.

Female: vaginitis, frothy discharge (white to green).

IAHI Block 1 (19 decks)

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